The ACSS2 Knockout CAL-27 Polyclonal Cells are a CRISPR/Cas9-edited heterogeneous population derived from the CAL-27 oral squamous cell carcinoma line, in which the acetyl-CoA synthetase ACSS2 gene has been disrupted to create a loss-of-function model. This polyclonal knockout pool retains population-level diversity, enabling the study of ACSS2-dependent phenotypes without clonal selection bias, and is ideal for examining gene-dosage effects or heterogeneous cancer cell behaviors.
The host CAL-27 cell line originates from a human tongue squamous cell carcinoma and displays adherent epithelial morphology. As a widely employed model of oral cancer, CAL-27 cells retain invasive properties and metabolic adaptability, recapitulating key aspects of head and neck tumor biology. This line is frequently utilized for investigations into nutrient stress responses, metabolic reprogramming, and drug resistance mechanisms.
ACSS2 (acetyl-CoA synthetase short-chain family member 2) catalyzes the conversion of acetate to acetyl-CoA, a metabolite central to lipid synthesis and histone acetylation. Its expression is induced by HIF1?? under hypoxia and by SREBF1 in response to lipogenic signals, while AMPK can suppress activity through phosphorylation. Acetyl-CoA generated by ACSS2 feeds into fatty acid biosynthesis via ACACA and FASN, and into epigenetic regulation through EP300/CREBBP-mediated histone acetylation, notably increasing H3K9ac and H3K27ac at promoters of oncogenes like MYC and CCND1. ACSS2 cooperates with ACLY and interacts with TFEB to maintain nucleocytosolic acetyl-CoA pools, positioning it as a metabolic hub that integrates nutrient availability with gene expression programs driving cell growth and survival.
In CAL-27 oral cancer cells, ACSS2 activity is essential for sustaining acetyl-CoA levels during hypoxia or nutrient limitation. Disruption of ACSS2 depletes acetyl-CoA, thereby curtailing de novo fatty acid synthesis and reducing histone acetylation at growth-promoting genes. This polyclonal knockout model consequently shows impaired proliferation, colony formation, and migration, especially under metabolic stress, highlighting the dependence of oral squamous cell carcinoma on acetate metabolism.
This ACSS2 knockout cell population is suitable for investigating acetate utilization, histone acetylation dynamics, and ACSS2-targeted therapy. Applications include western blot analysis of ACSS2 and H3K9ac/H3K27ac, RT?qPCR of FASN and ACC, LC?MS?based acetyl-CoA measurement, proliferation, colony formation, and Transwell assays, as well as ChIP?qPCR at MYC/CCND1 and metabolomic or drug?response studies. For technical inquiries or to order, contact Ascent Research.
